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Biomedical subjects

H Sumino

Publications and source records attributed to H Sumino.

At least 19 recordsLinked to original sources

Elevated arterial stiffness in postmenopausal women with osteoporosis.

OBJECTIVES: Osteoporosis and increased pulse wave velocity (PWV) are cardiovascular risk factors. We investigated the relationship between PWV and bone mass in the lumbar spine in postmenopausal women. METHODS: We studied the PWV in 95 women; 38 postmenopausal women with normal spinal bone mineral density (BMD), 32 osteopenic postmenopausal women, and 25 osteoporotic postmenopausal women. The brachial-ankle PWV (baPWV) was measured using an automated device. The BMD of the lumbar spine (L2-L4) was measured using dual-energy X-ray absorptiometry. RESULTS: After adjusting for age and years since menopause, women with osteoporosis had a significantly higher baPWV than those with normal BMD (1500 +/- 220 cm/s versus 1340 +/- 215 cm/s; P < 0.05), but no significant differences in baPWV were seen between the osteoporotic and osteopenic groups or between the osteopenic and normal BMD groups. In univariate regression analysis, the baPWV was significantly negatively correlated with BMD (r = -0.450, P < 0.01), and significantly positively correlated with age (r = 0.601, P < 0.01), years since menopause (r = 0.577, P < 0.01), systolic blood pressure (r = 0.295, P < 0.01), and diastolic blood pressure (r = 0.264, P < 0.05), but was not with other variables. In multivariate regression analysis, the baPWV was significantly correlated with BMD (P < 0.05), but not with other variables. CONCLUSIONS: Postmenopausal women with osteoporosis may have elevated arterial stiffness, suggesting that osteoporotic postmenopausal women may have a higher risk of cardiovascular disease.

Absorptiometry, Photon↗

Effects of torasemide on cardiac sympathetic nerve activity and left ventricular remodelling in patients with congestive heart failure.

OBJECTIVE: To determine the effect of torasemide, a loop diuretic with antialdosteronergic properties, compared with furosemide on cardiac sympathetic nerve activity in patients with congestive heart failure (CHF). METHODS: 40 patients with non-ischaemic CHF (left ventricular ejection fraction (LVEF) < 45%) were randomly assigned to torasemide (4-8 mg/day; n = 20) or furosemide (20-40 mg/day; n = 20). All patients were also treated with angiotensin-converting enzyme inhibitor. The delayed heart to mediastinum count (H/M) ratio, delayed total defect score (TDS) and washout rate were determined from iodine-123 meta-iodobenzylguanidine measured before and 6 months after treatment. Left ventricular end diastolic volume (LVEDV), left ventricular end systolic volume (LVESV) and LVEF were also determined by echocardiography. RESULTS: After treatment, in patients receiving torasemide, TDS decreased from 44 (8) to 36 (8) (p < 0.001), H/M ratio increased from 1.61 (0.19) to 1.77 (0.24) (p < 0.001), and washout rate decreased from 52 (12)% to 41 (14)% (p = 0.001). In addition, LVEDV decreased from 173 (22) ml to 147 (30) ml (p < 0.001) and LVESV decreased from 117 (19) ml to 95(24) ml (p < 0.001). Although LVEF tended to increase, the change was not significant (from 31 (7)% to 34 (7)%, NS). Conversely, these parameters did not change significantly in patients receiving furosemide. Moreover, percentage change of TDS was significantly correlated with percentage change of LVEDV (r = 0.473, p < 0.05) and of LVESV (r = 0.579, p < 0.01) after torasemide treatment. CONCLUSION: These findings indicate that torasemide treatment can ameliorate cardiac sympathetic nerve activity and left ventricular remodelling in patients with CHF.

Aged↗

Low strength wastewater treatment under low temperature conditions by a novel sulfur redox action process.

The objective of this research is to make a novel wastewater treatment process activated by a sulfur-redox cycle action of microbes in low temperature conditions. This action is carried out by sulfate-reducing bacteria (SRB) and sulfur-oxidizing bacteria (SOB). The process was comprised of a UASB reactor as pre-treatment and an aerobic downflow hanging sponge (DHS) reactor as post-treatment. As the results of reactor operation, the whole process achieved that over 90% of CODcr removal efficiency, less than 30 mgCODcr/L (less than 15 mgBOD/L) of final effluent, at 12 h of HRT and at 8 degrees C of UASB reactor temperature. Acetobacterium sp. was detected as the predominant species by PCR-DGGE method targeting 16SrDNA with band excision and sequence analysis. In the UASB reactor, various species of sulfate-reducing bacterium, Desulfobulbus sp., Desulfovibrio sp., and Desulfomicrobium sp., were found by cloning analysis. In the DHS reactor, Tetracoccus sp. presented as dominant. The proposed sulfur-redox action process was considered as an applicable process for low strength wastewater treatment in low temperature conditions.

Bioreactors↗

Comparative effects of valsartan and enalapril on cardiac sympathetic nerve activity and plasma brain natriuretic peptide in patients with congestive heart failure.

OBJECTIVE: To evaluate the effects of valsartan on cardiac sympathetic nerve activity, plasma brain natriuretic peptide (BNP) concentration, cardiac function, and symptoms in patients with congestive heart failure (CHF) by comparison with those of enalapril. METHODS: 50 patients with CHF (left ventricular ejection fraction (LVEF) < 40%) were randomly assigned to valsartan (80 mg/day; n = 25) or enalapril (5 mg/day; n = 25). All patients were also treated with a loop diuretic. The delayed heart to mediastinum count (H/M) ratio, delayed total defect score (TDS), and washout rate were determined from (123)I-meta-iodobenzylguanidine (MIBG) images. Plasma BNP concentrations were measured before and after six months of treatment. The left ventricular end diastolic volume (LVEDV) and LVEF were also determined by echocardiography. RESULTS: In patients receiving valsartan, TDS decreased from a mean (SD) of 43 (8) to 39 (10) (p < 0.01), H/M ratio increased from 1.70 (0.17) to 1.78 (0.22) (p < 0.05), washout rate decreased from 46 (11)% to 41 (10)% (p < 0.05), and plasma BNP concentration decreased from 237 (180) pg/ml to 143 (93) pg/ml (p < 0.05). In addition, LVEDV decreased from 172 (42) ml to 151 (45) ml (p < 0.05) and LVEF increased from 31 (7)% to 39 (10)% (p < 0.001). However, these parameters did not change significantly in patients receiving enalapril. CONCLUSION: Plasma BNP concentration and (123)I-MIBG scintigraphic and echocardiographic parameters improved significantly after six months of treatment with valsartan. These findings indicate that valsartan can improve cardiac sympathetic nerve activity and left ventricular performance in patients with CHF.

3-Iodobenzylguanidine↗

Conjugated estrogen plus medroxyprogesterone does not impair blood rheological properties in hypertensive postmenopausal women.

OBJECTIVES: Hypertension and estrogens are both prothrombotic. We used the microchannel method to investigate whether hormone replacement therapy (HRT) with conjugated equine estrogen (CEE) plus medroxyprogesterone acetate (MPA) affects blood flow through the microchannels in hypertensive postmenopausal women being treated with antihypertensive drugs and in normotensive postmenopausal women. METHODS: Sixty-two consecutive postmenopausal women were randomly assigned to a hypertensive HRT group (n=16), hypertensive control group (n=15), normotensive HRT group (n=16) and normotensive control group (n=15). Each HRT group received CEE 0.625 mg plus MPA 2.5 mg daily orally for 12 months. Both hypertensive groups were being treated with antihypertensive drugs before the study. Microvascular blood flow was assessed on the basis of blood passage time, the time required for 100 microl of whole blood to pass through a cylinder, was determined before and 12 months after the start of HRT by the microchannel method (micro channel array flow analyzer). RESULTS: CEE plus MPA therapy did not change blood passage time in any of the groups. Microscopic observation showed that the whole blood passed smoothly through the microchannels in every group. CONCLUSIONS: CEE plus MPA therapy may not impair blood flow through the microchannels in hypertensive postmenopausal women receiving antihypertensive drugs or in normotensive postmenopausal women. However, administration of CEE plus MPA to postmenopausal women with hypertension warrants caution against the occurrence of thromboembolic events.

Aged↗

Effects of hormone replacement therapy on weight, abdominal fat distribution, and lipid levels in Japanese postmenopausal women.

OBJECTIVE: To investigate the effects of hormone replacement therapy (HRT) on weight, abdominal fat distribution, and fasting lipid levels in Japanese postmenopausal women (PMW). DESIGN: Prospective, 12-month-controlled clinical comparison of women with and without HRT. SUBJECTS: In all, 35 PMW with HRT (conjugated estrogens, 0.625 mg daily; medroxyprogesterone acetate, 2.5 mg daily; HRT group) and 26 PMW without HRT (control group). MEASUREMENTS: Weight, abdominal fat distribution by computed tomographic measurements, lipid profiles, and sex hormones were determined at baseline and after 12 months of treatment or observation. RESULTS: Weight did not change in any group. Visceral abdominal fat increased in controls, but not in the HRT group. Total and low-density lipoprotein cholesterol decreased, and triglyceride (TG) and high-density lipoprotein cholesterol increased in the HRT group; these did not change in the control group. When we divided women into those with android and gynoid types of abdominal fat distribution. Subjects with an android distribution showed reduced visceral fat with HRT, which also decreased the proportion of patients maintaining an android distribution. HRT did not alter abdominal fat distribution in subjects with a gynoid distribution. HRT increased serum TG in the android and the gynoid subgroups. CONCLUSION: Improved distribution of abdominal fat and fasting lipid levels except for TG may represent beneficial effects of HRT with respect to cardiovascular disease, but caution is warranted concerning TG elevation from HRT performed in PMW.

Abdomen↗

Hormone replacement therapy increases plasma level of angiotensin II in postmenopausal hypertensive women.

The renin-angiotensin-aldosterone system plays a major role in the pathogenesis of hypertension by enhancing the production or the activity of angiotensin II (ANG II). We evaluated the effects of hormone replacement therapy (HRT) on the renin-angiotensin-aldosterone system and on bradykinin in postmenopausal women (PMW) who were hypertensive or normotensive. Subjects included 28 PMW whose elevated blood pressure (BP) was well controlled on antihypertensive agents excluding diuretics, angiotensin-converting enzyme (ACE) inhibitors, and ANG II receptor antagonists. As controls, we evaluated 16 normotensive PMW. All subjects received oral HRT daily for 6 months. The plasma levels of angiotensin I (ANG I), ANG II, and bradykinin as well as plasma renin activity (PRA) showed a significant increase in HRT in the hypertensive group, but not in the normotensive group. The serum ACE activity showed a significant decrease in both groups, but the plasma level of aldosterone was unchanged. Despite the decrease in serum ACE activity, there was an increase in the plasma ANG II level. Hormone replacement therapy increased the level of ANG II in the hypertensive women, but their BP was unaffected. The increase in plasma bradykinin level may maintain homeostasis in the presence of an increase in plasma ANG II, which is a risk factor for cardiovascular disease. Hormone replacement therapy was associated with a decrease in serum ACE and an increase in plasma bradykinin in hypertensive PMW. Accordingly, the protective effect of HRT against cardiovascular disease in PMW can be provided by a decrease in ACE activity and an increase in bradykinin.

Aldosterone↗

Troglitazone improves endothelial function and augments renal klotho mRNA expression in Otsuka Long-Evans Tokushima Fatty (OLETF) rats with multiple atherogenic risk factors.

Targeted disruption of the klotho gene induces multiple phenotypes characteristic of human aging, including arteriosclerosis, pulmonary emphysema and osteoporosis. Moreover, we previously observed that insufficient klotho expression in mice leads to endothelial dysfunction. In the present study, we used Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which exhibit hypertension, obesity, severe hyperglycemia and hypertriglyceridemia, and are thus considered an animal model of atherogenic disease, to test the effects of oral administration of troglitazone (200 mg/kg) on renal klotho mRNA expression and endothelial function. Systolic blood pressure, body weight, plasma glucose and triglyceride levels were all significantly higher in 30-week-old OLETF rats than in controls (LETO; Long-Evans Tokushima Otsuka) (p<0.05, n=7). In addition, endothelium-dependent relaxation of the aorta in response to 10(-5) M acetylcholine was significantly attenuated in OLETF rats (p<0.05, n=7), as was renal expression of klotho mRNA. Administration of troglitazone for 10 weeks significantly reduced systolic blood pressure, plasma glucose and triglyceride levels in OLETF rats, while augmenting endothelium-dependent aortic relaxation and renal klotho mRNA expression. These findings suggest that troglitazone protects the vascular endothelium against damage caused by the presence of multiple atherogenic factors.

Animals↗

Combined primary aldosteronism and preclinical Cushing's syndrome: an unusual case presentation of adrenal adenoma.

A 55-year-old woman was referred to our institution for evaluation of elevated plasma creatine phosphokinase, hypokalemia and hypertension. Her chief complaints were muscle weakness and polyuria. A left adrenal mass, 4 cm in diameter, was noted on computed tomography. Hormonal assessment demonstrated markedly elevated plasma aldosterone concentration, markedly low plasma renin activity, an abnormal diurnal variation in serum cortisol levels, suppressed baseline plasma adrenocorticotrophic hormone, and non-suppression of serum cortisol by dexamethasone suppression test. She showed no symptoms or signs suggestive of Cushing's syndrome. Adrenal scintigraphy with 131I-6-beta-iodomethyl-norcholesterol showed uptake on the left adrenal and inhibition of the contralateral adrenal gland. She was diagnosed with combined primary aldosteronism and preclinical Cushing's syndrome. Cases of combined primary aldosteronism and preclinical Cushing's syndrome are extremely rare. In patients with large aldosterone-producing adenoma, contralateral adrenal insufficiency should be anticipated after the removal of the tumor.

Adenoma↗

Reduction of viral myocarditis in mice lacking perforin.

Cellular immunity plays an important role and contributes to morbidity and mortality in the development of cardiomyopathy secondary to acute myocarditis. Lymphocytotoxicity has been proposed as due to infiltrated cytotoxic T lymphocytes (CTLs). Perforin is thought to be a major factor responsible for the cytolytic properties of the CTLs. To investigate whether mice lacking perforin have enhanced severity of viral myocarditis and acceleration of myocardial apoptosis, perforin knockout (KO) mice were infected with encephalomyocarditis virus. The average cardiac viral titer in perforin KO mice was not significantly different from that in the wild type mice. The heart weight/body weight ratio in perforin KO mice on days 4 and 12 were the same in the wild type mice (n=4 of each). Hearts in perforin KO mice were smaller than that in perforin + mice and grades of myocardial necrosis and lymphocyte infiltration were significantly reduced than in perforin + mice on day 12 after viral inoculation. In the perforin KO mice, the number of apoptotic cells was significantly higher than in wild type on day 4. Perforin blockade induced the early induction of myocardial apoptosis and suppressed the late onset of myocardial injury by cellular autoimmunity. Blockade of perforin gene expression at an early stage may limit viral myocarditis for therapeutic intervention.

Animals↗

[Hormone replacement therapy and vascular function].

Hormone replacement therapy (HRT) by estrogen has a cardioprotective effect in postmenopausal women. This effect results partly from the direct actions of estrogen on vascular receptors. These are mainly endothelium-dependent or endothelium-independent vascular relaxing effects. Increases in prostacyclin and bradykinin, and a decrease in endothelin-1 by estrogen are involved.

English Abstract↗

Serum level of vascular endothelial growth factor is decreased by hormone replacement therapy in postmenopausal women without hypercholesterolemia.

The administration of hormone replacement therapy (HRT) to postmenopausal women (PMW) reportedly has beneficial effects on their levels of lipid and lipoproteins. Estrogen retards the development of atherosclerosis induced by a high-fat diet in animals. Although vascular endothelial growth factor (VEGF) may be involved in the development of atherosclerosis in humans, there is no information on effect of estrogen administration on VEGF level and lipid metabolism. We evaluated 64 healthy normotensive or hypertensive PMW before and during the administration of HRT (0.625 mg conjugated equine estrogen combined with 2.5 mg medroxyprogesterone acetate orally) daily for 6 months. All hypertensive PMW were well-controlled on antihypertensive drug therapy. According to their total cholesterol level at baseline, we divided the PMW with HRT (n=54) into a normocholesterolemic group (NC, total cholesterol <220 mg/dl, n=35) and a hypercholesterolemic group (HC, total cholesterol >/=220 mg/dl, n=19). We evaluated the serum levels of VEGF at baseline, and again at 3 and 6 months after starting HRT. HRT significantly (P<0.01) reduced the mean VEGF level from 31.5+/-4.3 pg/ml at baseline to 18.2+/-2.3 pg/ml after 6 months in the NC group. However, the VEGF levels in the HC group and the control group exhibited no significant change at either 3 or 6 months after starting HRT. In summary, HRT, using a combination of conjugated equine estrogen and medroxyprogesterone acetate, reduced the level of VEGF in normocholesterolemic PMW more effectively than in those with hypercholesterolemia.

Aged↗

Mössbauer studies on laser evaporated iron atoms and their reactions with oxygen in argon matrices.

Laser-evaporated iron atoms were isolated in low-temperature Ar matrices and their chemical reactions with oxygen were investigated by means of Mössbauer spectroscopy. Reactions of iron atoms with oxygen produce FeO, Fe(O2), FeO3, (O2)FeO2 and OFeO isolated in the Ar matrices and their yields vary depending on the concentration of oxygen. Similarly, FeO and Fe(O2) were obtained by the reaction of iron atoms with N2O. Infrared spectroscopy and molecular orbital calculations were applied to support their assignments.

Calorimetry↗

Renal artery stenosis associated with epidermal nevus syndrome.

Epidermal nevus syndrome is an unusual neurocutaneous disorder in which epidermal nevi are associated with abnormalities of the skeleton and central nervous system, including the eyes and somtimes the cardiovascular system. We treated a patient in whom the latter included renal artery stenosis. An 18-year-old man with epidermal nevi was diagnosed as having the syndrome based on the additional presence of scoliosis, an arachnoid cyst in the middle cranial fossa, and microphthalmos. Hypertension was diagnosed when the patient was 15 years old. The plasma renin activity (9.7 ng/ml/h) was elevated. Right renal artery stenosis was demonstrated by angiography, and the abdominal aorta was narrowed distal to the ostium of the superior mesenteric artery. The plasma renin activity in the right renal vein (16 ng/ml/h) was higher than contralaterally (10 ng/ml/h). Several cardiovascular manifestations have been reported as a complication of epidermal nevus syndrome. Hypertension in an individual with epidermal nevi and congenital anomalies should prompt a search for a vascular anomaly.

Adolescent↗

Effect of enalapril on exhaled nitric oxide in normotensive and hypertensive subjects.

We investigated whether an angiotensin-converting enzyme (ACE) inhibitor increases the production of nitric oxide (NO) in exhaled air in normotensive and hypertensive subjects. In study 1, 8 normotensive male subjects received a single oral dose of enalapril (5 mg) or nitrendipine (10 mg) in a crossover manner. Exhaled air was collected at baseline, and at 2, 4, and 8 hours after administration of the drug. In study 2, 10 normotensive subjects (6 men and 4 women) and 10 hypertensive subjects (6 men and 4 women) received a single oral dose of enalapril (5 mg). Exhaled air was collected at baseline and at 2 and 4 hours after administration of the drug. In study 1, enalapril significantly increased the NO release rate from the lung in normotensive subjects (36.9+/-5.1 pmol/s at baseline versus 58.3+/-7.3 pmol/s at 4 hours, P<0.01). Nitrendipine did not change the NO release rate. In study 2, enalapril significantly increased the release of NO from the lung in normotensive subjects (40.4+/-6.0 pmol/s at baseline versus 70. 3+/-11.4 pmol/s at 4 hours, P<0.01) but not in hypertensive subjects. ACE inhibition increased NO production from the lung in normotensive subjects but not in hypertensive patients. The reduction of angiotensin II production and/or the accumulation of bradykinin in the pulmonary tissue may be responsible for increased NO production in components of the lung, such as the pulmonary vascular endothelium, bronchial epithelial cells, macrophages, nasopharyngeal cells, and neurons. However, the effects of ACE inhibition on NO production from the lung differ between hypertensive subjects and normotensive subjects.

Adult↗

Renovascular hypertension observed in a patient with antiphospholipid-antibody syndrome.

The antiphospholipid-antibody syndrome is associated with an increased incidence of arterial and venous thrombosis. Although renal infarction has been observed in these patients, stenotic lesions of the renal artery associated with the antiphospholipid-antibody syndrome have not been reported. A 47-year-old male with a history of hypertension for 7 years developed blurred vision secondary to thrombotic occlusion of the central retinal artery. Laboratory and radiologic examinations revealed renal dysfunction, a positive anticardiolipin antibody, and narrowing of the right renal artery. Successful percutaneous transluminal renal artery angioplasty resulted in normalization of the blood pressure and recovery of renal function.

Angioplasty, Balloon, Coronary↗

Effects of antihypertensive therapy on blood pressure and left ventricular hypertrophy in patients with severe hypertension.

The mechanisms responsible for regression of left ventricular (LV) mass with antihypertensive therapy in patients with severe hypertension remain unclear. This study was designed to examine whether systolic and diastolic blood pressures are associated with changes in LV mass. Eighteen patients with essential hypertension whose average seated diastolic blood pressure was >or = 110 mm Hg were enrolled in the study. All patients were administered antihypertensive therapy and underwent M-mode echocardiography before and after 6 months of treatment. In all patients, antihypertensive treatment significantly reduced systolic blood pressure from 175 +/- 21 mm Hg at baseline to 143 +/- 22 mm Hg at 6 months (p < 0.001), and diastolic blood pressure from 116 +/- 7 mm Hg at baseline to 92 +/- 20 mm Hg at 6 months (p < 0.001). LV mass index at 6 months was significantly reduced compared to its baseline value (p < 0.05). Change (value at 6 months-value at baseline) in systolic and diastolic blood pressures correlated positively with the change in LV mass index (r = 0.61, p < 0.01 and r = 0.71, p < 0.001, respectively). The patients were divided into responders. whose LV mass regressed by > or = 10% (n = 9), and nonresponders, whose LV mass regressed by < 10% (n = 9). Systolic (p < 0.001) and diastolic (p < 0.001) blood pressures. interventricular septal thickness (p< 0.05), posterior wall thickness (p < 0.001), and LV mass index (p < 0.001) were significantly decreased in the responders, but not in the nonresponders, at 6 months compared with those at baseline. Systolic (p < 0.05) and diastolic (p < 0.05) blood pressures in nonresponders were significantly higher than those in the responders at 6 months. The changes in systolic and diastolic blood pressures did not correlate with the change in LV mass index in the responders or the nonresponders. The regression of LV mass is strongly affected by reducing blood pressure. This is the first study using antihypertensive therapy to demonstrate that a change in blood pressure correlates positively with changes in LV mass index in severely hypertensive patients.

Adult↗

Positive correlation between circulating leptin levels and lipid lipoproteins in postmenopausal women administered hormone replacement therapy.

Beneficial effects of hormone replacement therapy are reported on plasma concentrations of lipids and lipoproteins. Plasma leptin levels are reported to reflect lipid metabolism. We treated 40 healthy postmenopausal women with continuous combined HRT (0.625 mg conjugated equine estrogen and 2.5 mg medroxyprogesterone acetate orally) daily for 6 months and then investigated total cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) cholesterol, which are considered to be factors inducing cardiovascular disease (CVD). We measured the plasma levels of lipids and leptin, which are considered to be altered with HRT. Plasma leptin and lipid levels were measured at baseline and after 3 and 6 months of HRT. The plasma levels of leptin in PMW were not significantly reduced by HRT. Although the plasma levels of total cholesterol and LDL-cholesterol did not change by HRT, the administration of HRT significantly increased plasma levels of triglycerides and HDL-cholesterol in PMW. The correlation between leptin and total cholesterol or triglycerides was positive after HRT while these relations were not correlated at baseline. The correlation between lipid levels and leptin may explain the new role of leptin in plasma lipid levels in HRT.

Aged↗